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Antiarrhythmic
Drugs
Dr. Hiwa K. Saaed PhD Pharmacology
Antiarrhythmic Drugs
• Antiarrhythmic drugs Prevent or treat irregularities of cardiac
rhythm
• Half of all cardiac deaths are due to cardiac arrhythmias
• Arrhythmias are due to a disturbance of the electrical
impulses which regulate the heart.
• cardiac arrhythmias may require RX, because the heart that
are beat…………..CAN REDUCE CARDIAC OUTPUT
1. too slowly (bradycardia)
2. too rapidly (tachycardia),
3. regularly (sinus tachycardia or sinus bradycardia)
4. Or irregularly (atrial fibrillation).
• The normal heart rate is between 60-100 beats/ minute
What is an Arrhythmia?
The arrhythmias are conceptually simple-dysfunctions cause
abnormalities in
– impulse formation (abnormal automaticity)
– conduction in the myocardium (reentry),
– or combination of both.
However, in the clinic, arrhythmias present as a complex family of
disorders that show a variety of symptoms.
Normal heartbeat and atrial arrhythmia
Normal rhythm Atrial arrhythmia
AV septum
To function efficiently, heart needs to contract sequentially (atria, then
ventricles) and in synchronicity: SA node→ atrial muscle → AV node
(0.15 sec) → bundle of His → Purkinje fibers → ventricular (0.1 sec)
Therefore Arrhythmia is defined as any rhythm that does not start at
the SA node Or that is not under the usual autonomic control
The heart cavity from which the arrhythmia originates
gives the name to the arrhythmia
Supraventricular
• Ectopic (Extrasystole or PC)
(atrial or AV nodal)
• Tachycardia (atrial or AV
nodal)
• Atrial fibrillation and flutter
Ventricular
• Ectopic (Extrasystole or PC)
• Tachycardia
• Ventricular fibrillation and
flutter
NB: more than 3 Ectopic impulses are called tachycardia otherwise
they are called premature contraction
Cardiac arrhythmias
Arrhythmias are a frequent
problem in clinical practice,
occurring in up to:
– 25% of patients treated
with digitalis
– 50% of anesthetized
patients
– 80% of patients with MI
• are often associated with
hyperthyroidism and
electrolyte disorders
Factors that precipitate of
arrhythmia
– Cardiac ischemia,
– Hypoxia,
– Acidosis, alkalosis
– Electrolyte disturbances
– Excessive catecholamine
exposure
– Exposure to toxic
substances
– Unknown etiology
Cardiac electrophysiology
The heart is self-excitable, initiating its own rhythmic contractions,1% autorhythmic
cell” SA & AV node, they don’t contract:, SLOW response, Slow upstroke velocity ,
a smaller magnitude of AP and a brief plateau, No fast Na+ channel, the AP is
caused by Ca+2
99% contractile cells,
FAST response
The basic events that occur during the formation of the action potential :
Cardiac Action Potential
• Divided into five phases (0,1,2,3,4)
– Phase 4 - Diastole depolarization
the resting membrane potential is maintained by K+ efflux
and slow Na+ & Ca2+ influx
• Except for the SA node, the heart rests.
• Addition of current into cardiac muscle (stimulation) causes
– Phase 0 – rapid depolarization- opening of fast Na+
channels
• Drives Na+ into cell (inward current), changing
membrane potential
• Transient outward current due to movement of Cl- and K+
Cardiac Action Potential (con’t)
Phase 1 – initial rapid repolarization
– Closure of the fast Na+ channels
– it is followed by a brief and incomplete period of
repolarization.
– K+ efflux: This period is mediated by a temporary
movement of K+ from the intracellular to the extracellular
space.
– Cl- influx.
– Phase 0 and 1 together correspond to the R and S waves of
the ECG
• Phase 2 - plateau phase
– sustained by the balance between Ca+ influx and K + efflux
– Unique to the cardiac action potential
– Normally blocks any premature stimulator signals (other
muscle tissue can accept additional stimulation and increase
contractility in a summation effect)
– This initiates a slow repolarization, and creates a plateau in
the action potential. Cardiac contraction is mediated by
phase 2.
– Corresponds to ST segment of the ECG.
Cardiac Action Potential (con’t)
• Phase 3 – rapid repolarization
– The calcium channels close. The process of repolarization is
accelerated.
– K+ channels remain open, Allows K+ to build up outside the
cell, causing the cell to repolarize
– K + channels finally close when membrane potential
reaches certain level
– Corresponds to T wave on the ECG
Cardiac Action Potential (con’t)
ECG (EKG) showing wave segments
Contraction of atria
Contraction of
ventricles
Repolarization of
ventricles
The electrical
events that occur in
the heart are
reflected in the
ECG waveform.
Normal ECG
• The P wave: atrial depolarization.
• The PR interval: the amount of time the electrical impulse
takes to travel from the SA node through the AV node (0.12
to 0.2 seconds).
• The QRS represents the amount of time it takes the
ventricles to depolarize. In normal conduction, ventricular
depolarization occurs rapidly; this rapid conduction is
reflected in a narrow QRS interval (< 0.1 sec).
• The T wave represents ventricular repolarization.
• The QT interval : time that it takes the ventricles to
depolarize and repolarize; start of the QRS complex to the
end of repolarization (or the end of the T wave).
• The normal QT interval is <.44 sec.
Abnormal ECG Waveform
• During the early part of the QT interval, the ventricles are
completely refractory and unable to respond to another
electrical impulse.
• During the latter part of the interval, the ventricles are only
partially refractory and may respond to some impulses but not
to others.
Abnormal ECG Waveform
• When changes occur in the normal cardiac cycle, the normal
ECG waveform is altered to reflect them.
For example,
• prolonged QT interval: prolonged ventricular repolarization.
• prolonged PR interval: A slowing of conduction from the SA
node through the AV node.
• QRS that is wider than usual or bizarre in shape: Abnormal
conduction of the electrical impulse through the ventricles.
1. Disorders of impulse formation
(Abnormal automaticity):
• The SA node shows the fastest rate of Phase 4 depolarization,
• However, if cardiac sites other than the SA node show enhanced
automaticity, they may generate competing stimuli, and
arrhythmias may arise.
• Cardiac myopathy: Abnormal automaticity may also occur if the
myocardial cells are damaged (for example, by hypoxia or
potassium imbalance).
2. Disorders of impulse conduction
May result in abnormality in rate:
– Bradycardia (if have AV block)
– Tachycardia (if reentrant circuit occurs)
Reentrant
circuit
State-dependent use
• Therapeutically useful channel-blocking drugs bind readily to
– activated channels (ie, during phase 0)
– or inactivated channels (ie, during phase 2)
• but bind poorly or not at all to rested channels.
• Therefore, these drugs block electrical activity when there is
a fast tachycardia rized tissue.
Cardiac Na+ channels
BASIC PHARMACOLOGY OF THE ANTIARRHYTHMIC
AGENTS
• Biggest problem – antiarrhythmics can cause
arrhythmia!
– Example: Treatment of a non-life threatening tachycardia may cause
fatal ventricular arrhythmia
– Must be vigilant in determining dosing, blood levels, and in follow-up
when prescribing antiarrhythmics
• Arrhythmias are caused by abnormal pacemaker activity or
impulse propagation. Thus, the aim of therapy is to:
1. reduce ectopic pacemaker activity
2. and modify conduction or refractoriness in reentry circuits to disable
circus movement.
Therapeutic overview
Vaughan Williams classification
1. Na+ channel blockade Class I
2. β-adrenergic receptor blockade Class II
3. Prolong repolarization Class III
4. Ca2+ channel blockade Class IV
Miscellaneous
• Adenosine
• Digitalis glycosides
• K+
• Mg2+
Classification of antiarrhythmic drugs
Drugs Mechanism of action comment
IA Na+ Channel blocker Moderately Slows phase 0 depolarization in
ventricle APD and ERP
IB Na+ Channel blocker Shortens phase 3 repolarization in ventricle APD
and ERP
IC Na+ Channel blocker Markedly Slows phase 0 depolarization in ventricle
no effect on APD and ERP
II Β adrenergic blocker Inhibits phase 4 depolarization in SA and AV nodes
III K+ Channel blocker Prolongs Phase 3 repolarization in ventricle APD
and ERP
IV Ca+2 Channel blocker Inhibits action potential in SA and AV nodes
Class I – blocker’s of fast Na+ channels
• Subclass IA
– Cause moderate Phase 0 depression
– Prolong repolarization
– Increased duration of action potential
– Includes
• Quinidine – 1st antiarrhythmic used, treat both atrial and
ventricular arrhythmias, increases refractory period
• Procainamide - increases refractory period but side
effects
• Disopyramide – extended duration of action, used only
for treating ventricular arrhythmias
Class I – blocker’s of fast Na+ channels
Quinidine-
indications and MOA
• Indication: both VA and SVA
• Blocks activated Na+ channel: ↓slope of phase 0 and 4
• Inhibit K+ current:↑phase 3
• Both above effects ↑ Action potential ↑ QT interval
• α-blocking  vasodilation reflex tachycardia
• Antimuscarinic effect
Pharmacokinetics and Drug Interactions
• ~80% bound to plasma protein, metabolized by liver; interacts with enzyme
inducer and inhibitors
1. ↑digoxin plasma level displace it from tissue and ↓renal excretion.
2. ↑ plasma level of oral anticoagulant & barbiturates.
Quinidine-
adverse effects
Cardiac Adverse effects:
• torsade depoints (↑QT interval) twisting of peak in ECG
• Proarrhythmogenic effects, AV block or asystole (toxic dose)
Extracardiac Adverse effects:
• GIT; DNV
• Cinchonism: headache, dizziness, confusion, tinnitus,
deafness, blurring of vision
• Quinidine syncope because of VA (↑QT);
• light headedness and fainting
Procainamide
• Both VA, SVA (less sensistive) & PVCs
• Orally, IV & IM
• Electrophysiological effects are similar to Quinidine.
• Less antimuscarinic
• but more ganglionic blocking effects.
Procainamide- adverse effects
• Lupus erythromatous-like syndrome; rash, small joints
arthralgia & arthritis
• Pleuritis & pericarditis
• Hypotension because of ?
• Toxic dose:
• Asystole, Torsade de points, Hallucination & psychosis
Disopyramide
• Both VA & SVA (Treatment and Prophylaxis)
• Orally & I.V
• Very similar to Quinine EXCEPT more Negative inotropic
and antimuscarinic effects
• Less side effects & allergy than Quinidine
Adverse effects
• Cardiac toxicity similar to quinidine
• Torsade de points
• HF because of negative inotropic effects
• Antimuscarinic effects: dry mouth, urinary retention,
constipation,
Contraindications: glaucoma, BPH,
• Weak Phase 0 depression
• Shortened depolarization
• Decreased action potential duration
– Lidocaine (also acts as local anesthetic) – blocks Na+
channels mostly in ventricular cells, also good for digitalis-
associated arrhythmias
– Mexiletine - oral lidocaine derivative, similar activity
– Phenytoin – anticonvulsant that also works as
antiarrhythmic similar to lidocaine
Subclass IB: Lidocaine, mexiletine, tocainide, phenytoin
Subclass IB: Lidocaine, mexiletine, tocainide, phenytoin
Class IB-Lidocaine
• t1/2 1-1.5 hr given by I.V loading dose followed by I.V infusion
• Block both activated & inactivated Na+ channel
• ↓The slope of phase 0 & 4
• No ECG changes in PR & QRS
Main uses:
• VA following MI and local anesthesia
NB: Reduce the dose in liver disease and heart failure
Adverse Effects:
CNS: drowsiness, numbness, parathesia, slurred speeches, difficulty of
swallowing, convulsions, nystagmus, tremor, Diplopia
Heart: AV block, ↓contractility
Class IB: Tocainide & Mexilitine
Are congeners of lidocaine, and they can be administered orally, resist to 1st
pass effects
Mexilitine has also shown significant efficacy in relieving chronic
pain, especially due to diastolic hypertrophy & nerve injury
Mexiletine is used for chronic treatment of ventricular
arrhythmias associated with previous MI.
Tocainide is used for treatment of ventricular tachyarrhythmias.
cause pulmonary fibrosis & liver toxic, much less used
Cardiac: Bradycardia, Av block, hypotension, ventricular
tachycardia
Extracardiac: anorexia, nausea, tremor, Pulmonary fibrosis & bone
marrow aplasia
Phenytoin
• An anticonvulsant that bind to inactivated Na+ channel and
prolong the inactivated state
• Long t1/2, zero order kinetic difficult to use
Drug of choice for Treatment:
• Ventricular arrhythmia
• digoxin-induced atrial and ventricular Arrhythmia
Adverse effects: gingival hyperplasia, ataxia
• Strong Phase 0 depression
• No effect of depolarization
• No effect on action potential duration
• Flecainide (initially developed as a local anesthetic)
– Potent blocker of Na+ shorten AP
– Potent blocker of K+ prolong AP
– Net result no change
– Slows conduction in all parts of heart,
– Also inhibits abnormal automaticity
Proarrhytmogenic : reserved for life threatening SVA & VA in
pts without myocardial structural abnormalities
Subclass IC: flecainide, propafenone, moricizine
Subclass IC: flecainide, propafenone, moricizine
Class IC- Flecainide, Propafenone & moricizine
• Propafenone
– Has some structural similarities to propranolol
– Weak β – blocker
– Also some Ca2+ channel blockade
– Also slows conduction
– VA & SVA: its spectrum of action similar to that flecainide
– AE: metallic taste & constipation
• Moricizine
– Derivative of phenothiazine
– Mechanism of action similar to flecainide-VA
– Proarrhythmogenic
Class 1 A, B & C
Class I ↓Conduction ERP Automaticity Contraction Site ECG
change
IA Moderate ↑ Depressed by all
More marked for
abnormal foci
depressed VA &SVA ↑QT
IB Minimal ↓ No Only VA ─
IC v. marked ─ depressed VA &SVA ↑QT
Class II – β–adrenergic blockers
• Based on two major actions
1) blockade of myocardial β–adrenergic receptors↓cAMP
 ↓ both Na+ & Ca+ current
2) Direct membrane-stabilizing effects related to Na+ channel
blockade
↓both automaticity & HR and suppression of abnormal
pacemaker activity
– The AV node is particularly sensitive to β-blockers
– The PR interval is usually prolonged by β-blockers
Class II- β–adrenergic blockers
Propranolol
– Slows SA node and ectopic pacemaking
– Can block arrhythmias induced by exercise or
apprehension
– Other β–adrenergic blockers have similar therapeutic
effect
– Metoprolol ,Nadolol, Atenolol, Acebutolol,
Pindolol, Sotalol, Timolol; prophylactic in MI
– Esmolol (very short acting; I.V exclusively for acute
surgical arrhythmia)
• Toxicities: pts with arrhythmias are more prone to decrease in
COP induced by these drugs than are pts with normal heart
Class III – K+ channel blockers
Developed because some patients negatively sensitive to Na+
channel blockers (they died!)
Cause delay in repolarization and prolonged refractory period
Includes: Sotalol, Ibutilide are prototype
Amiodarone – markedly prolongs action potential by delaying K+
efflux but many other effects characteristic of other classes
Ibutilide – slows inward movement of Na+ in addition to delaying
K + influx.
Bretylium – is an older drug that combines general
sympathoplegic actions & a K+ channel blocking effects in
ischemic tissues, first developed to treat hypertension but found
to also suppress VF associated with MI
Dofetilide - is a newer K+ channel blocker prolongs action
potential by delaying K+ efflux with no other effects
Class III – K+ channel blockers
Class III – K+ channel blockers
Class III (sotalol, Ibutilide, amiodarone, dofetilide) & class I
(quinidine & NAPC) prolong the AP duration ↑ERP prevent
tachycardia ↑QT interval
Bretylim also produces AP prolongation but causes little ECG
change
• Bretylium is used for refractory VF & V tachycardia during
times of cardiac arrest
• AE: postural hypotension, arrhythmogenic
Sotalol: effective in both SVA & VA 80-320mg/ daily/oral
• AE; tdp, sinus brady cardia, asthma
• Ibutilide and Dofetilide are recommended for A. flutter and
A. fibrilation
• AE: tdp
Class III-Amiodarone
• Structurally related to thyroid hormone
• Effective in most types of arrhythmias & is most efficacious of
all antiarrhythmic, because of toxicities, mainly used in
arrhythmias that are resistant to other drugs.
• Blocks Na+, Ca+2 & K+ channels and α-& β-receptors
• Marked prolongs the QT interval & QRS duration, it increases
Atrial, AV and Ventricular refractory period
Clinicali use: Long term but last choose.
• In patients with AF there is no time for admin of digoxin
because of long t1/2
• As alternative for DC shock when not available
• The best to control WPW syndrome
Amiodarone-adverse effects
• Toxicity because of accumulation
• Hepatic, cardiac, pulmonary fibrosis 20%
• Thyroid hypo- or hyperthyroidism
• Skin photosensitivity-blue discoloration
• Nerves peripheral neuritis
• Corneal deposits
• Kidney not involved
• ↑Digoxin level
• NB. Rarely cause new arrhythmia b Ca+2, Na+, K+ and α-& β-
blockade
Class IV – L-Ca2+ channel blockers
Verapamil & diltiazem
• slow rate of AV-conduction in patients with atrial
fibrillation
• ↑ERP  ↑PR interval
• Includes
– Verapamil – blocks Na+ channels in addition to Ca2+; also
slows SA node in tachycardia
Suppression of SA node; bradycardia
Slowing of AV node: abolish AV reentry
– Diltiazem
Class IV: Drug of choice for SVA: A flutter and fibrillation b?
Class IV – L-Ca2+ channel blockers Verapamil & diltiazem
Miscellaneous
Adenosine I.V bolus (6-12 mg) V. effective, short t1/2 15 secs
• Markedly slows or completely blocks conduction in AV node*
Probably by hyperpolarizing this tissue through ↑K+ (Ach-
sensitive K + channel in SA & AV node) and ↓Ca+2 currents
• DOC for SVT due to* replaced verapamil for this use
• AE: flushing, hypotension, dyspnea, chest pain
Digitalis: rapid atrial or AV nodal arrhythmias atrial flutter and
atrial fibrillation.
• K+ depress ectopic pacemaker including those caused by
digitalis
• Mg+2 effective in some cases of tdp and digitalis induced
arrhythmia
Effects on Conduction, Refractory Period and ECG
Class
ECG
PR
ECG
QRS
ECG
QT
Conduction
velocity
Refractory
Period
IA +/0 + ++ ↓, ↑ (low dose) ↑
IB 0 0 0/- No/little ↓ ↓
IC + ++ + Much ↓ No/little ↓
II ++ 0 0 ↓ in SAN/AVN ↑ in SAN/AVN
III 0 0 ++ No effect ↑↑
IV ++ 0 0 ↓ in SAN/AVN ↑ in SAN/AVN

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Antiarrythmic drugs

  • 1. Antiarrhythmic Drugs Dr. Hiwa K. Saaed PhD Pharmacology
  • 2. Antiarrhythmic Drugs • Antiarrhythmic drugs Prevent or treat irregularities of cardiac rhythm • Half of all cardiac deaths are due to cardiac arrhythmias • Arrhythmias are due to a disturbance of the electrical impulses which regulate the heart. • cardiac arrhythmias may require RX, because the heart that are beat…………..CAN REDUCE CARDIAC OUTPUT 1. too slowly (bradycardia) 2. too rapidly (tachycardia), 3. regularly (sinus tachycardia or sinus bradycardia) 4. Or irregularly (atrial fibrillation). • The normal heart rate is between 60-100 beats/ minute
  • 3. What is an Arrhythmia? The arrhythmias are conceptually simple-dysfunctions cause abnormalities in – impulse formation (abnormal automaticity) – conduction in the myocardium (reentry), – or combination of both. However, in the clinic, arrhythmias present as a complex family of disorders that show a variety of symptoms.
  • 4. Normal heartbeat and atrial arrhythmia Normal rhythm Atrial arrhythmia AV septum To function efficiently, heart needs to contract sequentially (atria, then ventricles) and in synchronicity: SA node→ atrial muscle → AV node (0.15 sec) → bundle of His → Purkinje fibers → ventricular (0.1 sec) Therefore Arrhythmia is defined as any rhythm that does not start at the SA node Or that is not under the usual autonomic control
  • 5. The heart cavity from which the arrhythmia originates gives the name to the arrhythmia Supraventricular • Ectopic (Extrasystole or PC) (atrial or AV nodal) • Tachycardia (atrial or AV nodal) • Atrial fibrillation and flutter Ventricular • Ectopic (Extrasystole or PC) • Tachycardia • Ventricular fibrillation and flutter NB: more than 3 Ectopic impulses are called tachycardia otherwise they are called premature contraction
  • 6. Cardiac arrhythmias Arrhythmias are a frequent problem in clinical practice, occurring in up to: – 25% of patients treated with digitalis – 50% of anesthetized patients – 80% of patients with MI • are often associated with hyperthyroidism and electrolyte disorders Factors that precipitate of arrhythmia – Cardiac ischemia, – Hypoxia, – Acidosis, alkalosis – Electrolyte disturbances – Excessive catecholamine exposure – Exposure to toxic substances – Unknown etiology
  • 7. Cardiac electrophysiology The heart is self-excitable, initiating its own rhythmic contractions,1% autorhythmic cell” SA & AV node, they don’t contract:, SLOW response, Slow upstroke velocity , a smaller magnitude of AP and a brief plateau, No fast Na+ channel, the AP is caused by Ca+2 99% contractile cells, FAST response
  • 8.
  • 9. The basic events that occur during the formation of the action potential :
  • 10. Cardiac Action Potential • Divided into five phases (0,1,2,3,4) – Phase 4 - Diastole depolarization the resting membrane potential is maintained by K+ efflux and slow Na+ & Ca2+ influx • Except for the SA node, the heart rests. • Addition of current into cardiac muscle (stimulation) causes – Phase 0 – rapid depolarization- opening of fast Na+ channels • Drives Na+ into cell (inward current), changing membrane potential • Transient outward current due to movement of Cl- and K+
  • 11. Cardiac Action Potential (con’t) Phase 1 – initial rapid repolarization – Closure of the fast Na+ channels – it is followed by a brief and incomplete period of repolarization. – K+ efflux: This period is mediated by a temporary movement of K+ from the intracellular to the extracellular space. – Cl- influx. – Phase 0 and 1 together correspond to the R and S waves of the ECG
  • 12. • Phase 2 - plateau phase – sustained by the balance between Ca+ influx and K + efflux – Unique to the cardiac action potential – Normally blocks any premature stimulator signals (other muscle tissue can accept additional stimulation and increase contractility in a summation effect) – This initiates a slow repolarization, and creates a plateau in the action potential. Cardiac contraction is mediated by phase 2. – Corresponds to ST segment of the ECG. Cardiac Action Potential (con’t)
  • 13. • Phase 3 – rapid repolarization – The calcium channels close. The process of repolarization is accelerated. – K+ channels remain open, Allows K+ to build up outside the cell, causing the cell to repolarize – K + channels finally close when membrane potential reaches certain level – Corresponds to T wave on the ECG Cardiac Action Potential (con’t)
  • 14. ECG (EKG) showing wave segments Contraction of atria Contraction of ventricles Repolarization of ventricles The electrical events that occur in the heart are reflected in the ECG waveform.
  • 15. Normal ECG • The P wave: atrial depolarization. • The PR interval: the amount of time the electrical impulse takes to travel from the SA node through the AV node (0.12 to 0.2 seconds). • The QRS represents the amount of time it takes the ventricles to depolarize. In normal conduction, ventricular depolarization occurs rapidly; this rapid conduction is reflected in a narrow QRS interval (< 0.1 sec). • The T wave represents ventricular repolarization. • The QT interval : time that it takes the ventricles to depolarize and repolarize; start of the QRS complex to the end of repolarization (or the end of the T wave). • The normal QT interval is <.44 sec.
  • 16. Abnormal ECG Waveform • During the early part of the QT interval, the ventricles are completely refractory and unable to respond to another electrical impulse. • During the latter part of the interval, the ventricles are only partially refractory and may respond to some impulses but not to others. Abnormal ECG Waveform • When changes occur in the normal cardiac cycle, the normal ECG waveform is altered to reflect them. For example, • prolonged QT interval: prolonged ventricular repolarization. • prolonged PR interval: A slowing of conduction from the SA node through the AV node. • QRS that is wider than usual or bizarre in shape: Abnormal conduction of the electrical impulse through the ventricles.
  • 17. 1. Disorders of impulse formation (Abnormal automaticity): • The SA node shows the fastest rate of Phase 4 depolarization, • However, if cardiac sites other than the SA node show enhanced automaticity, they may generate competing stimuli, and arrhythmias may arise. • Cardiac myopathy: Abnormal automaticity may also occur if the myocardial cells are damaged (for example, by hypoxia or potassium imbalance).
  • 18. 2. Disorders of impulse conduction May result in abnormality in rate: – Bradycardia (if have AV block) – Tachycardia (if reentrant circuit occurs) Reentrant circuit
  • 19. State-dependent use • Therapeutically useful channel-blocking drugs bind readily to – activated channels (ie, during phase 0) – or inactivated channels (ie, during phase 2) • but bind poorly or not at all to rested channels. • Therefore, these drugs block electrical activity when there is a fast tachycardia rized tissue. Cardiac Na+ channels
  • 20. BASIC PHARMACOLOGY OF THE ANTIARRHYTHMIC AGENTS • Biggest problem – antiarrhythmics can cause arrhythmia! – Example: Treatment of a non-life threatening tachycardia may cause fatal ventricular arrhythmia – Must be vigilant in determining dosing, blood levels, and in follow-up when prescribing antiarrhythmics • Arrhythmias are caused by abnormal pacemaker activity or impulse propagation. Thus, the aim of therapy is to: 1. reduce ectopic pacemaker activity 2. and modify conduction or refractoriness in reentry circuits to disable circus movement.
  • 21. Therapeutic overview Vaughan Williams classification 1. Na+ channel blockade Class I 2. β-adrenergic receptor blockade Class II 3. Prolong repolarization Class III 4. Ca2+ channel blockade Class IV Miscellaneous • Adenosine • Digitalis glycosides • K+ • Mg2+
  • 22. Classification of antiarrhythmic drugs Drugs Mechanism of action comment IA Na+ Channel blocker Moderately Slows phase 0 depolarization in ventricle APD and ERP IB Na+ Channel blocker Shortens phase 3 repolarization in ventricle APD and ERP IC Na+ Channel blocker Markedly Slows phase 0 depolarization in ventricle no effect on APD and ERP II Β adrenergic blocker Inhibits phase 4 depolarization in SA and AV nodes III K+ Channel blocker Prolongs Phase 3 repolarization in ventricle APD and ERP IV Ca+2 Channel blocker Inhibits action potential in SA and AV nodes
  • 23. Class I – blocker’s of fast Na+ channels • Subclass IA – Cause moderate Phase 0 depression – Prolong repolarization – Increased duration of action potential – Includes • Quinidine – 1st antiarrhythmic used, treat both atrial and ventricular arrhythmias, increases refractory period • Procainamide - increases refractory period but side effects • Disopyramide – extended duration of action, used only for treating ventricular arrhythmias
  • 24. Class I – blocker’s of fast Na+ channels
  • 25. Quinidine- indications and MOA • Indication: both VA and SVA • Blocks activated Na+ channel: ↓slope of phase 0 and 4 • Inhibit K+ current:↑phase 3 • Both above effects ↑ Action potential ↑ QT interval • α-blocking  vasodilation reflex tachycardia • Antimuscarinic effect Pharmacokinetics and Drug Interactions • ~80% bound to plasma protein, metabolized by liver; interacts with enzyme inducer and inhibitors 1. ↑digoxin plasma level displace it from tissue and ↓renal excretion. 2. ↑ plasma level of oral anticoagulant & barbiturates.
  • 26. Quinidine- adverse effects Cardiac Adverse effects: • torsade depoints (↑QT interval) twisting of peak in ECG • Proarrhythmogenic effects, AV block or asystole (toxic dose) Extracardiac Adverse effects: • GIT; DNV • Cinchonism: headache, dizziness, confusion, tinnitus, deafness, blurring of vision • Quinidine syncope because of VA (↑QT); • light headedness and fainting
  • 27. Procainamide • Both VA, SVA (less sensistive) & PVCs • Orally, IV & IM • Electrophysiological effects are similar to Quinidine. • Less antimuscarinic • but more ganglionic blocking effects. Procainamide- adverse effects • Lupus erythromatous-like syndrome; rash, small joints arthralgia & arthritis • Pleuritis & pericarditis • Hypotension because of ? • Toxic dose: • Asystole, Torsade de points, Hallucination & psychosis
  • 28. Disopyramide • Both VA & SVA (Treatment and Prophylaxis) • Orally & I.V • Very similar to Quinine EXCEPT more Negative inotropic and antimuscarinic effects • Less side effects & allergy than Quinidine Adverse effects • Cardiac toxicity similar to quinidine • Torsade de points • HF because of negative inotropic effects • Antimuscarinic effects: dry mouth, urinary retention, constipation, Contraindications: glaucoma, BPH,
  • 29. • Weak Phase 0 depression • Shortened depolarization • Decreased action potential duration – Lidocaine (also acts as local anesthetic) – blocks Na+ channels mostly in ventricular cells, also good for digitalis- associated arrhythmias – Mexiletine - oral lidocaine derivative, similar activity – Phenytoin – anticonvulsant that also works as antiarrhythmic similar to lidocaine Subclass IB: Lidocaine, mexiletine, tocainide, phenytoin
  • 30. Subclass IB: Lidocaine, mexiletine, tocainide, phenytoin
  • 31. Class IB-Lidocaine • t1/2 1-1.5 hr given by I.V loading dose followed by I.V infusion • Block both activated & inactivated Na+ channel • ↓The slope of phase 0 & 4 • No ECG changes in PR & QRS Main uses: • VA following MI and local anesthesia NB: Reduce the dose in liver disease and heart failure Adverse Effects: CNS: drowsiness, numbness, parathesia, slurred speeches, difficulty of swallowing, convulsions, nystagmus, tremor, Diplopia Heart: AV block, ↓contractility
  • 32. Class IB: Tocainide & Mexilitine Are congeners of lidocaine, and they can be administered orally, resist to 1st pass effects Mexilitine has also shown significant efficacy in relieving chronic pain, especially due to diastolic hypertrophy & nerve injury Mexiletine is used for chronic treatment of ventricular arrhythmias associated with previous MI. Tocainide is used for treatment of ventricular tachyarrhythmias. cause pulmonary fibrosis & liver toxic, much less used Cardiac: Bradycardia, Av block, hypotension, ventricular tachycardia Extracardiac: anorexia, nausea, tremor, Pulmonary fibrosis & bone marrow aplasia
  • 33. Phenytoin • An anticonvulsant that bind to inactivated Na+ channel and prolong the inactivated state • Long t1/2, zero order kinetic difficult to use Drug of choice for Treatment: • Ventricular arrhythmia • digoxin-induced atrial and ventricular Arrhythmia Adverse effects: gingival hyperplasia, ataxia
  • 34. • Strong Phase 0 depression • No effect of depolarization • No effect on action potential duration • Flecainide (initially developed as a local anesthetic) – Potent blocker of Na+ shorten AP – Potent blocker of K+ prolong AP – Net result no change – Slows conduction in all parts of heart, – Also inhibits abnormal automaticity Proarrhytmogenic : reserved for life threatening SVA & VA in pts without myocardial structural abnormalities Subclass IC: flecainide, propafenone, moricizine
  • 35. Subclass IC: flecainide, propafenone, moricizine
  • 36. Class IC- Flecainide, Propafenone & moricizine • Propafenone – Has some structural similarities to propranolol – Weak β – blocker – Also some Ca2+ channel blockade – Also slows conduction – VA & SVA: its spectrum of action similar to that flecainide – AE: metallic taste & constipation • Moricizine – Derivative of phenothiazine – Mechanism of action similar to flecainide-VA – Proarrhythmogenic
  • 37. Class 1 A, B & C Class I ↓Conduction ERP Automaticity Contraction Site ECG change IA Moderate ↑ Depressed by all More marked for abnormal foci depressed VA &SVA ↑QT IB Minimal ↓ No Only VA ─ IC v. marked ─ depressed VA &SVA ↑QT
  • 38. Class II – β–adrenergic blockers • Based on two major actions 1) blockade of myocardial β–adrenergic receptors↓cAMP  ↓ both Na+ & Ca+ current 2) Direct membrane-stabilizing effects related to Na+ channel blockade ↓both automaticity & HR and suppression of abnormal pacemaker activity – The AV node is particularly sensitive to β-blockers – The PR interval is usually prolonged by β-blockers
  • 39. Class II- β–adrenergic blockers Propranolol – Slows SA node and ectopic pacemaking – Can block arrhythmias induced by exercise or apprehension – Other β–adrenergic blockers have similar therapeutic effect – Metoprolol ,Nadolol, Atenolol, Acebutolol, Pindolol, Sotalol, Timolol; prophylactic in MI – Esmolol (very short acting; I.V exclusively for acute surgical arrhythmia) • Toxicities: pts with arrhythmias are more prone to decrease in COP induced by these drugs than are pts with normal heart
  • 40. Class III – K+ channel blockers Developed because some patients negatively sensitive to Na+ channel blockers (they died!) Cause delay in repolarization and prolonged refractory period Includes: Sotalol, Ibutilide are prototype Amiodarone – markedly prolongs action potential by delaying K+ efflux but many other effects characteristic of other classes Ibutilide – slows inward movement of Na+ in addition to delaying K + influx. Bretylium – is an older drug that combines general sympathoplegic actions & a K+ channel blocking effects in ischemic tissues, first developed to treat hypertension but found to also suppress VF associated with MI Dofetilide - is a newer K+ channel blocker prolongs action potential by delaying K+ efflux with no other effects
  • 41. Class III – K+ channel blockers
  • 42. Class III – K+ channel blockers Class III (sotalol, Ibutilide, amiodarone, dofetilide) & class I (quinidine & NAPC) prolong the AP duration ↑ERP prevent tachycardia ↑QT interval Bretylim also produces AP prolongation but causes little ECG change • Bretylium is used for refractory VF & V tachycardia during times of cardiac arrest • AE: postural hypotension, arrhythmogenic Sotalol: effective in both SVA & VA 80-320mg/ daily/oral • AE; tdp, sinus brady cardia, asthma • Ibutilide and Dofetilide are recommended for A. flutter and A. fibrilation • AE: tdp
  • 43. Class III-Amiodarone • Structurally related to thyroid hormone • Effective in most types of arrhythmias & is most efficacious of all antiarrhythmic, because of toxicities, mainly used in arrhythmias that are resistant to other drugs. • Blocks Na+, Ca+2 & K+ channels and α-& β-receptors • Marked prolongs the QT interval & QRS duration, it increases Atrial, AV and Ventricular refractory period Clinicali use: Long term but last choose. • In patients with AF there is no time for admin of digoxin because of long t1/2 • As alternative for DC shock when not available • The best to control WPW syndrome
  • 44. Amiodarone-adverse effects • Toxicity because of accumulation • Hepatic, cardiac, pulmonary fibrosis 20% • Thyroid hypo- or hyperthyroidism • Skin photosensitivity-blue discoloration • Nerves peripheral neuritis • Corneal deposits • Kidney not involved • ↑Digoxin level • NB. Rarely cause new arrhythmia b Ca+2, Na+, K+ and α-& β- blockade
  • 45. Class IV – L-Ca2+ channel blockers Verapamil & diltiazem • slow rate of AV-conduction in patients with atrial fibrillation • ↑ERP  ↑PR interval • Includes – Verapamil – blocks Na+ channels in addition to Ca2+; also slows SA node in tachycardia Suppression of SA node; bradycardia Slowing of AV node: abolish AV reentry – Diltiazem Class IV: Drug of choice for SVA: A flutter and fibrillation b?
  • 46. Class IV – L-Ca2+ channel blockers Verapamil & diltiazem
  • 47. Miscellaneous Adenosine I.V bolus (6-12 mg) V. effective, short t1/2 15 secs • Markedly slows or completely blocks conduction in AV node* Probably by hyperpolarizing this tissue through ↑K+ (Ach- sensitive K + channel in SA & AV node) and ↓Ca+2 currents • DOC for SVT due to* replaced verapamil for this use • AE: flushing, hypotension, dyspnea, chest pain Digitalis: rapid atrial or AV nodal arrhythmias atrial flutter and atrial fibrillation. • K+ depress ectopic pacemaker including those caused by digitalis • Mg+2 effective in some cases of tdp and digitalis induced arrhythmia
  • 48. Effects on Conduction, Refractory Period and ECG Class ECG PR ECG QRS ECG QT Conduction velocity Refractory Period IA +/0 + ++ ↓, ↑ (low dose) ↑ IB 0 0 0/- No/little ↓ ↓ IC + ++ + Much ↓ No/little ↓ II ++ 0 0 ↓ in SAN/AVN ↑ in SAN/AVN III 0 0 ++ No effect ↑↑ IV ++ 0 0 ↓ in SAN/AVN ↑ in SAN/AVN